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Two neural mechanisms for respiration-induced cutaneous vasodilatation in humans?

Journal article
Authors Gunnar B Wallin
K Båtelsson
P Kienbaum
T Karlsson
B Gazelius
M Elam
Published in The Journal of physiology
Volume 513 ( Pt 2)
Pages 559-69
ISSN 0022-3751
Publication year 1998
Published at Institute of Clinical Neurosciences
Pages 559-69
Language en
Keywords Adult, Cold Temperature, Female, Fingers, physiology, Foot, blood supply, innervation, Hot Temperature, Humans, Male, Nervous System Physiological Phenomena, Norepinephrine, antagonists & inhibitors, Respiration, Skin, blood supply, innervation, Skin Temperature, physiology, Sympathetic Nervous System, metabolism, Vascular Resistance, physiology, Vasoconstriction, physiology, Vasodilation, physiology
Subject categories Cardiovascular medicine


1. In humans, a deep breath is known to induce cutaneous vasoconstriction in the warm state, and vasodilatation in the cold state. To investigate whether vasodilatation in the cold state is related to reduction of sympathetic vasoconstrictor nerve traffic, we studied the effect of a deep breath on vascular resistance in a skin area on the dorsum of the hand, in which release of noradrenaline from sympathetic nerves was blocked by iontophoretic pretreatment with bretylium tosylate. Simultaneous measurements were made in two control areas. In eight healthy subjects, data were obtained from deep breaths taken before bretylium in the warm state, after general cooling to a finger skin temperature below 25 C and after rewarming to above 32 C. 2. In the warm state before bretylium pretreatment, the deep breath evoked short-lasting vasoconstrictions at all sites. In the cold state there was no change of vascular resistance in the bretylium-pretreated area, whereas in the control areas an initial tendency towards vasoconstriction was followed by a significant transient vasodilatation. After rewarming, transient vasoconstrictions reappeared at the control sites, whereas only a transient vasodilatation occurred at the bretylium-pretreated site. 3. In six healthy subjects we also monitored the effects of a deep breath on skin sympathetic nerve activity (recorded by microneurography in the peroneal nerve), and skin vascular resistance within the innervation zone of the impaled nerve fascicle in the foot. Data from thirty deep breaths per subject were averaged. 4. In the cold state, the deep breath induced a strong increase in neural discharge, followed by a transient reduction of nerve traffic lasting approximately 15 s and associated with a subsequent reduction of vascular resistance. 5. We conclude that the deep breath-induced vasodilatation in the cold state is due to reduction of sympathetic vasoconstrictor nerve traffic. The vasodilatation after bretylium treatment in the warm state raises the possibility that a deep breath induces two simultaneous neural reactions, a vasoconstrictor and an active vasodilator component, the latter being weaker and normally masked by the strong vasoconstrictor component.

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